Recent studies have indicated that renal nerve activity may directly enhance renal tubular sodium reabsorption without altering renal perfusion pressure, renal blood flow, glomerular filtration rate or filtration fraction. The effect is believed to be due to a direct effect of norepinephrine released from sympathetic adrenergic nerve endings as this neurogenically mediated antinaturesis is abolished by alpha receptor blockade with phenoxybenzamine or pretreatment with guanethidine. Electron microscopy has been used to show that these nerve endings are in direct contact with the basement membrane of both proximal and distal tubular cells. In the dog, increases in renal nerve activity have been achieved by direct electrical stimulation or reflex stimulation induced by either acute arterial hemorrhage or a decrease in isolated carotid sinus pressure. Similar studies in the rat have demonstrated that the enhanced sodium reabsorption occurs primarily in the proximal tubule. The purpose of this study is to determine if a neurogenic pathway for the control of sodium reabsorption exists in Yucatan miniature swine, an animal who cardiovascular and renal control systems appear to be analogous to those in man. Studies designed to reflexly increase renal nerve traffic, and consequently sodium reabsorption by altering baroreceptor, thermoreceptor, and chemoreceptor input will be conducted. The role of the renal nerves in maintaining overall sodium balance in chronically instrumented conscious miniature swine will also be assessed under conditions of normal and low sodium intake.